ArticleAnnals of surgical treatment and research2021
Selective inhibition of V600E-mutant BRAF gene induces apoptosis in thyroid carcinoma cell lines.
Article in Annals of surgical treatment and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Treatment with Kinase Inhibitors Plus Myo-Inositol as Re-Differentiating Agents in Iodine-Refractory Thyroid Cancers.Life (Basel, Switzerland) · 2026Article
- The effect of glycolytic enzyme expression and thyroiditis on the aggressiveness of papillary thyroid carcinoma: a retrospective cohort study.Annals of surgical treatment and research · 2025Article
- Article
- BRAF-activated WT1 contributes to cancer growth and regulates autophagy and apoptosis in papillary thyroid carcinoma.Journal of translational medicine · 2022Article
- Novel Inhibitor-Based Therapies for Thyroid Cancer-An Update.International journal of molecular sciences · 2021Review
- Genetic Variants Associated with Thyroid Cancer Risk: Comprehensive Research Synopsis, Meta-Analysis, and Cumulative Epidemiological Evidence.Journal of oncology · 2021Review
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
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Abstract
purposePapillary thyroid cancer (PTC) has a high incidence of BRAF
methodsTwo thyroid cancer cell lines TPC1 and 8505C were treated with PLX4032, an analysis was done on cell growth, cell cycle, the degree of apoptosis, and levels of inflammatory cytokines. To identify the functional links of BRAF, we used the STRING database.
resultsDocking results illustrated PLX4032 blocked the kinase activity by exclusively binding on the serine/threonine kinase domain. STRING results indicated BRAF is functionally linked to mitogen-activated protein kinase. Both cell lines showed a dose-dependent reduction in growth rate but had a different half maximal inhibitory concentration value for PLX4032. The reaction to PLX4032 was more sensitive in the 8505C cells than in the TPC1 cells. PLX4032 induced a G2/M phase arrest in the TPC1 cells and G0/G1 in the 8505C cells. PLX4032 induced apoptosis only in the 8505C cells. With PLX4032, the TPC1 cells showed decreased levels of vascular endothelial growth factor, granulocyte-macrophage colony-stimulating factor, chemokine (C-C motif) ligand 2/monocyte chemoattractant protein 1, whereas the 8505C cells showed significantly decreased levels of IL-8, serpin E1/plasminogen activator inhibitor-1, and matrix metalloproteinase (MMP)-3.
conclusionPLX4032 was cytotoxic in both TPC1 and 8505C cells and induced apoptosis. In the 8505C cells, inflammatory cytokines such as IL-8 and MMP-3 were down-regulated. These findings suggest the possibility that the BRAF
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